I've only used the SNS caps but have done two separate cycles. It's more of a long term effect but I felt like it definitely helped. I can't pinpoint it exactly since I used it with other products but the literature on it squashes any doubts of mine.

TTA 3g daily (the last 500mg before bed)
ALCAR 10g daily (5g on wake up and the another 5g before bed)
RK (1-1.5g daily)

and you will SEE the diference

Tetradecylthioacetic acid (TTA) is a structurally modified form of fatty acid known as a 3-thia fatty acid. Thia fatty acids are saturated fatty acids which are modified by inserting a sulfur atom at a specific position in the carbon backbone. In the case of TTA, the sulfur atom is inserted in the 3-position of the carbon backbone, hence the classification as a "3"-thia fatty acid.

The oxidation of fatty acids occurs in the mitochondria of the cell through a process known as beta oxidation. The entire process of fatty acid metabolism involves multiple steps in which fats are first mobilized from storage sites and ultimately "burned" for energy. Although TTA itself is not processed through beta oxidation, it does stimulate the beta oxidation of other fatty acids (Berge and Hvattum, 1994). It is important to note that in addition to stimulating the oxidation of other fatty acids, TTA has been shown to result in an increase in actual mitochondria, as well as an increase in gene expression of some key enzymes involved in fatty acid oxidation (Totland et al., 2000). This is important as the amount of mitochondria and enzymes involved in fatty acid metabolism may be associated with the overall rate of lipid oxidation.
In previous work mitochondrial growth has been shown to be induced in both type I (slow twitch) and type II (fast twitch) skeletal muscle fibers, as well as in the diaphragm (Totland et al., 2000). Moreover, TTA increased the gene expression of carnitine palmitoyltranserferase II in the diaphragm, an enzyme crucial for the transport of activated fatty acids inside the mitochondria to undergo beta oxidation. Taken together, these effects of TTA on mitochondrial growth and gene expression may prove beneficial to the end result of increased fat oxidation. However, it should be noted that similar to the majority of studies using TTA as a therapeutic agent, the work of Totland et al. (2000) used rats that were fed these modified fatty acids. Replicated work in human subjects administered the same therapeutic dosages is necessary before conclusions can be drawn in relation to the impact of TTA on fatty acid oxidation in human subjects.

Fatty Acid Oxidation and TTA

As mentioned above, although TTA itself is not oxidized through beta oxidation, it has been shown to stimulate the beta oxidation of other fatty acids (Berge and Hvattum, 1994) and is clearly involved in lipid transport and utilization (Berge et al., 2005). This suggests that TTA may promote greater fatty acid usage and hence, greater fat loss over time. This may be partly due to the observation that TTA increases the transport of fatty acids into the mitochondria to undergo beta oxidation, as well as enhancing the process of beta oxidation itself (Madsen et al., 1999), which appears most prevalent in the liver (Berge et al., 2005). Related to this, several studies have reported on the beneficial effects of TTA administration related to fatty acid oxidation.
Skrede and Bremer (1993) noted that a single morning dosage of TTA (100mg) in rats increased fatty acid oxidation in isolated liver cells to values 3x greater than control (non-TTA treated) within 6 hours. Other work supports the role of TTA in increasing fatty acid oxidation, in addition to an increase in the production of ketones, which can be used as a fuel source (Madsen et al., 2002). Related to these findings, TTA has been shown to impart a significant effect on lowering blood lipids (total and LDL cholesterol), with a noted 56% reduction in VLDL-triacylglycerol (Asiedu et al., 1996). Similar effects have been noted in human subjects with HIV, in addition to a decrease in inflammation with TTA supplementation (Fredriksen et al., 2004). The effect on blood lipids may be partly related to the increase in fatty acid oxidation coupled with an increased gene expression for LDL receptors, which function in the removal of LDL cholesterol from circulation (Fredriksen et al., 2004). Such findings may have significant implications related to cardiovascular health.
Aside from the increase in fatty acid oxidation and the improvement in the blood lipid profile, TTA has been reported to prevent adiposity (accumulation of excess fat tissue) and to prevent insulin resistance, when rats were fed a high fat diet (Madsen et al., 2002). In this interesting study, it was noted that TTA treatment completely prevented the dietary-induced insulin resistance that is typically observed when animals consume a high fat diet, as well as prevented the accumulation of excess fat. This is an important finding, as insulin resistance is strongly associated with impaired glucose tolerance, often leading to obesity and the development of type II diabetes. The potential mechanism of action for these effects involves transcription factors known as peroxisome proliferators-activated receptors (PPAR), of which three distinct subtypes have been identified (alpha, gamma, delta/beta). The activation of these receptors by TTA (in particular PPARα) appears to be associated with the positive effects on gene activation related to enzymes involved in fatty acid transport and oxidation (Larsen et al., 2005).

Tetradecylthioacetic acid (TTA) is a non-beta-oxidizable fatty acid analog, which potently regulates lipid homeostasis. Here we evaluate the ability of TTA to prevent diet-induced and genetically determined adiposity and insulin resistance. In Wistar rats fed a high fat diet, TTA administration completely prevented diet-induced insulin resistance and adiposity. In genetically obese Zucker (fa/fa) rats TTA treatment reduced the epididymal adipose tissue mass and improved insulin sensitivity. All three rodent peroxisome proliferator-activated receptor (PPAR) subtypes were activated by TTA in the ranking order PPARalpha > PPARdelta > PPARgamma. Expression of PPARgamma target genes in adipose tissue was unaffected by TTA treatment, whereas the hepatic expression of PPARalpha-responsive genes encoding enzymes involved in fatty acid uptake, transport, and oxidation was induced. This was accompanied by increased hepatic mitochondrial beta-oxidation and a decreased fatty acid/ketone body ratio in plasma. These findings indicate that PPARalpha-dependent mechanisms play a pivotal role, but additionally, the involvement of PPARalpha-independent pathways is conceivable. Taken together, our results suggest that a TTA-induced increase in hepatic fatty acid oxidation and ketogenesis drains fatty acids from blood and extrahepatic tissues and that this contributes significantly to the beneficial effects of TTA on fat mass accumulation and peripheral insulin sensitivity.

PMID: 11971945 [PubMed - indexed for MEDLINE]

Department of Clinical Biology, University of Bergen, Norway

Administration of tetradecylthioacetic acid (a 3-thia fatty acid) increases mitochondrial and peroxisomal beta-oxidative capacity and carnitine palmitoyltransferase activity, but reduces free fatty acid and triacylglycerol levels in plasma compared to palmitic acid-treated rats and controls. The decrease in plasma triacylglycerol was accompanied by a reduction (56%) in VLDL-triacylglycerol. Prolonged supplementation of tetradecylthioacetic acid caused a significant increase in lipogenic enzyme activities (ATP-citrate lyase and acetyl-CoA carboxylase) and diacylglycerol acyltansferase, but did not affect phosphatidate phosphohydrolase. Plasma cholesterol, LDL- and HDL-cholesterol levels were reduced. 3-Hydroxy-3-methylglutaryl-coenzyme A reductase activity was, however, stimulated in 3-thia fatty acid-treated rats compared to controls. In addition. the mRNAs of 3-hydroxy-3-methylglutaryl-coenzyme A reductase and LDL-receptor were increased. Tetradecylthioacetic acid administration affected the fatty acid composition in plasma and liver by increasing the amount of monoenes, especially 18:1(n-9), mostly at the expense of omega-3 fatty acids. Compared to liver a large amount of tetradecylthioacetic acid accumulated in the heart, and this accumulation was accompanied by an increase in omega-3 fatty acids, particularly 22:6(n-3) and a decrease in omega-6 fatty acids, mainly 20:4(n-6). The results show that the hypolipidemic effect of tetradecylthioacetic acid is sustained after prolonged administration and may, at least in part, be due to increased fatty acid oxidation and upregulated LDL-receptor gene expression. The increase in lipogenic enzyme activities as well as increased 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity, may be compensatory mechanisms to maintain cellular integrity. Decreased level of 20:4(n-6) combined with increased omega-3/omega-6 ratio in cardiac tissue after tetradecylthioacetic acid treatment may have influence on membrane dynamics and function.

Tetradecylthioacetic acid a 3-thia fatty acid, is a novel bioactive compound. Besides being an antioxidant, it changes the plasma profile from atherogenic to cardioprotective

Tetradecylthioacetic acid (TTA) which can not be ▀-oxidized, lowers plasma VLDL-triacylglycerol (TG) and LDL-cholesterol (Chol). Increased mitochondrial ▀-oxidation with a concomitant decrease in TG synthesis and secretion, seems to be the primary mechanism underlying the hypotriglyceridemic effect not only of TTA but also of w-3 fatty acids as well as fibrates in rats, rabbits, dogs and possibly also in humans. TTA is an inhibitor of HMG-CoA reductase. We have generated results both in vivo and in vitro that present evidence that TTA besides being a lipid lowering agent, also possesses antioxidant properties. First, TTA inhibits the oxidative modification of LDL which is considered as the key step in the formation of foam cells and in initiation and progression of atherosclerotic plaque. Also TTA changes the antioxidant defense system in a beneficial way i.e. glutathion (GSH) is increased, the total antioxidant status is elevated and TBARS are decreased. Second, TTA has an │olive oil▓ effect since the plasma was enriched with oleic acid (18:1 n-9) and a É9-desaturated metabolite of TTA. This was due to upregulation of the hepatic enzyme É9-desaturase gene expression. Third, TTA lowers the plasma homocysteine level and inhibits restenosis. Fourth, TTA reduces the proliferation of smooth muscle cells. In conclusion, TTA is a hypolipidemic drug but also a new antioxidant. This novel bioactive compound is promising as a new therapeutic drug against atherosclerosis as it changes the plasma profile from atherogenic to cardioprotective.

Institute of Medicine, The Lipid Research Group, Haukeland University Hospital, University of Bergen, 5021 Bergen, Norway. rolf.berge@med.uib.no

Abstract
Much data indicates that lowering of plasma triglyceride levels by hypolipidemic agents is caused by a shift in the liver metabolism towards activation of peroxisome proliferator activated receptor (PPAR)alpha-regulated fatty acid catabolism in mitochondria. Feeding rats with lipid lowering agents leads to hypolipidemia, possibly by increased channeling of fatty acids to mitochondrial fatty acid oxidation at the expense of triglyceride synthesis. Our hypothesis is that increased hepatic fatty acid oxidation and ketogenesis drain fatty acids from blood and extrahepatic tissues and that this contributes significantly to the beneficial effects on fat mass accumulation and improved peripheral insulin sensitivity. To investigate this theory we employ modified fatty acids that change the plasma profile from atherogenic to cardioprotective. One of these novel agents, tetradecylthioacetic acid (TTA), is of particular interest due to its beneficial effects on lipid transport and utilization. These hypolipidemic effects are associated with increased fatty acid oxidation and altered energy state parameters of the liver. Experiments in PPAR alpha-null mice have demonstrated that the effects hypolipidemic of TTA cannot be explained by altered PPAR alpha regulation alone. TTA also activates the other PPARs (e.g., PPAR delta) and this might compensate for deficiency of PPAR alpha. Altogether, TTA-mediated clearance of blood triglycerides may result from a lowered level of apo C-III, with a subsequently induction of hepatic lipoprotein lipase activity and (re)uptake of fatty acids from very low density lipoprotein (VLDL). This is associated with an increased hepatic capacity for fatty acid oxidation, causing drainage of fatty acids from the blood stream. This can ultimately be linked to hypolipidemia, anti-adiposity, and improved insulin sensitivity.

Department of Biochemistry and Molecular Biology, University of Bergen, Norway. morten.elholm@pki.uib.no
Abstract
Administration of the fatty acid analogue tetradecylthioacetic acid (TTA) to rodents up-regulates peroxisomal and mitochondrial lipid-metabolizing enzymes and induces a proliferation of these organelles in hepatocytes. We show here that male NMRI mice fed a diet containing 0.3% (w/w) TTA revealed a transient two-fold increase in the incorporation of [3H]thymidine into the liver mtDNA followed by a 1.6-fold increase in the content of mtDNA. In addition, a transient three-fold increase in the mitochondrial thymidine kinase (TK2) activity and a slight increase in the DNA polymerase gamma activity was observed, indicating that the TTA induced mitochondrial proliferation is linked to an up-regulation of the mitochondrial thymidine kinase activity.

Abstract
Morphological and biochemical effects were induced at the subcellular level in the skeletal muscle, heart and liver of male rats as a result of feeding with EPA, DHA, and 3-thia fatty acids. The 3-thia fatty acid, tetradecylthioacetic acid (TTA) and EPA induced mitochondrial growth in type I muscle fibers in both the diaphragm and soleus muscle, and the size distribution of mitochondrial areas followed a similar pattern. Only the 3-thia fatty acid induced mitochondrial growth in type II muscle fibers. The mean area occupied by the mitochondria and the size distribution of mitochondrial areas in both fiber types were highly similar in DHA-treated and control animals. Only the 3-thia fatty acid increased the gene-expression of carnitine palmitoyltransferase (CPT)-II in the diaphragm. In the heart, however, the gene expression decreased. In hepatocytes an increase in the mean size of mitochondria was observed after EPA treatment, concomitant with an increase in mitochondrial CPT-II gene expression. Administration of 2-methyl-substituted EPA (methyl-EPA) induced a higher rate of growth of mitochondria than EPA. At the peroxisomal level in the hepatocytes a 3-thia fatty acid, EPA, and DHA increased the areal fraction concomitant with the induction of gene expression of peroxisomal fatty acyl-CoA oxidase (FAO). In the diaphragm, mRNA levels of FAO were not affected by EPA or DHA treatment, whereas gene expression was significantly increased after 3-thia fatty acid treatment. In the heart, both 3-thia fatty acid, EPA and DHA tended to decrease the levels of FAO mRNA. The areal fraction of fat droplets in all three tissue types was significantly lower in the groups treated with 3-thia fatty acid. In the group treated with EPA a lower areal fraction of fat droplets was observed, while the DHA group was similar to the control. This indicates that EPA and DHA have different effects on mitochondrial biogenesis.

The Lipid Research Group, Institute of Medicine, University of Bergen, Haukeland University Hospital, N-5021 Bergen, Norway. nkjgu@uib.no

The effects on oxidation and composition of fatty acids in rat liver were compared after administration of fatty acids with sulfur substituted in different positions. It has been hypothesized that drugs with hydrophobic backbone have lipid-lowering effects because they are not easily catabolized by mitochondrial beta-oxidation. Thia fatty acids cannot be beta-oxidized when sulfur is in 3-position, but beta-oxidation is possible when sulfur is positioned further from the carboxyl group. To investigate whether catabolism of thia fatty acids would affect their ability to influence lipid metabolism, a series of thia fatty acids were synthesized and administered by oral gavage to male Wistar rats (300 mg/kg bodyweight/day for 7 days). Depending on the position of the sulfur atom and the chain length, the thia fatty acids were beta-oxidized, desaturated and/or elongated, and the accumulated amounts were lower as the sulfur atom were positioned further from the carboxyl group. All thia fatty acids led to high peroxisomal beta-oxidation of endogenous fatty acids, whereas the mitochondrial beta-oxidation was high when sulfur was in 3-position, low when sulfur was in 4-position and similar to controls when sulfur was in 5- or 7-position. The changes in hepatic fatty acid composition were more pronounced when sulfur was positioned close to the carboxyl group. In conclusion, both the position of the sulfur atom and the chain length appear to determine the catabolic fate of thia fatty acids, and the non-beta-oxidizable thia fatty acids were most potent in regulating oxidation and composition of endogenous fatty acids in rat liver.

I've been dosing 2-3 caps TTA (sns) preWO with ArA (XFA) for about 4 weeks now, that stuff makes me sweat big time! (like dripping sweat just from holding a plank position for 30-45 secs when warming up) Just added in 2g LCLT this morning (along with AnaBeta)...and might add in a cap in the afternoon, possibly with some AT2, see how well it scares the fat off...

I have some 3,4 but PP suggested not to use it as it may free estrogen as well and can cause gyno issues but before I used AH I was using 3,4 I started 10 grams alcar today 5 grams before gym am 5 grams pm but so far just feel sick from the taste :/

I have some 3,4 but PP suggested not to use it as it may free estrogen as well and can cause gyno issues but before I used AH I was using 3,4 I started 10 grams alcar today 5 grams before gym am 5 grams pm but so far just feel sick from the taste :/

yeap it may freeing up some hormones like Test, DHT and Estrogen but protect the prostate from the negative effects of DHT. (if you above 1g of AH)

I've had some good luck with it so far, and would definitely stack it with other supps. The big thing I notice is that the lbs are dropping a bit easier than prior. No issues with cramping or anything.

I've had some good luck with it so far, and would definitely stack it with other supps. The big thing I notice is that the lbs are dropping a bit easier than prior. No issues with cramping or anything.

I've had some good luck with it so far, and would definitely stack it with other supps. The big thing I notice is that the lbs are dropping a bit easier than prior. No issues with cramping or anything.

Def good stuff! And remind me, you've been consistenly dosing 1g/day (1/1)...or did you bump it up to 3 caps (1.5g) a day?

Isn't this the popular ingredient foundin DCP? If so people loved that stuff and this is way cheaper.

Yep, at 250 mg, 100 mg of raspberry ketones, and a couple other things. Our TTA has each capsule at 500mg and we also have raspberry ketones at both 125 and 500 mg capsules for individual dosing preference. Not a knock on DCP at all because I think it is a good product. We just offer many of the effective ingredients individually, which allows for greater modification to dosages to allow for more individual flexibility and stacking options.

Been on stims for two years straight now, stacking two at a time for past year.. Looking to go stim free for two months during winter but not lose metabolic benefits.. Would tta be considered stim free? Could I use it with revamp to reset my bodies stim tolerance?? What about alphat2 + tta ? Thanks!

Been on stims for two years straight now, stacking two at a time for past year.. Looking to go stim free for two months during winter but not lose metabolic benefits.. Would tta be considered stim free? Could I use it with revamp to reset my bodies stim tolerance?? What about alphat2 + tta ? Thanks!

Been on stims for two years straight now, stacking two at a time for past year.. Looking to go stim free for two months during winter but not lose metabolic benefits.. Would tta be considered stim free? Could I use it with revamp to reset my bodies stim tolerance?? What about alphat2 + tta ? Thanks!